These beats are characterized by a QRS complex that is premature (relative to the baseline R-R cycle) but, in general, morphologically similar to normal sinus complexes (Fig. 6.1). The complex may thus be narrow or, if there is an associated bundle-branch block (BBB), wide ectopic beats are referred to as atrial (if there is a P wave differing in morphology and axis from the sinus P wave and a PR interval of ≥120 ms) or junctional (when there is a negative P wave in the inferior leads and a PR interval of <120 ms or no atrial deflection at all). Supraventricular ectopic beats (SVEBs) can occur singly or in groups. They are generally followed by an incomplete or noncompensatory pause (i.e., one lasting less than twice as long as the normal P-P cycle), which is the result of SA node depolarization by the ectopic impulse. If the atrial extrasystole is very premature, it may reach the AV node while the latter is still refractory, and in this case it will not be conducted to the ventricles (nonconducted premature atrial complex or blocked atrial extrasystole). If instead the refractoriness is encountered in one of the bundle branches, the supraventricular impulse will be conducted with a QRS configuration unlike that of the baseline tracing, i.e., resembling that associated with bundle branch block (aberrantly conducted supraventricular extrasystole) (Fig. 6.2). SVEBs can also trigger short bursts of atrial tachycardia (Fig. 6.3).

If the premature complex is morphologically different from that of the baseline tracing (i.e., wide QRS complex) and not preceded by an atrial wave, the extrasystole is ventricular in origin. These ventricular ectopic beats (VEBs) may occur in isolated form, in bigeminal or trigeminal patterns (characterized by a VEB after every one or two sinus beats, respectively) (Fig. 6.4a), or in couplets or triplets. (The rapid succession of three or more VEBs with a rate >100 bpm is usually referred to as unsustained ventricular tachycardia [VT].) VEBs are followed by a compensatory pause (i.e., one that is twice as long as the previous R-R cycle) (Fig. 6.4a), because in most cases the extrasystole does not depolarize the SA node, and the latter continues to emit impulses at its own discharge rate. Sometimes, however, the VEB fails to retrogradely penetrate the AV node or penetration is incomplete: in these cases the postextrasystolic sinus impulse will be conducted to the ventricles with a slight delay, as compared with normal atrioventricular conduction (Fig. 6.4b). When the rates of the normal and ectopic QRS complexes are similar, the morphology of the complexes may be intermediate between that observed during a normally conducted rhythm and that of the ectopic beat (fusion complex) (Fig. 6.4c). Particular attention should be reserved for premature VEBs falling near the peak of the previous T wave (the R-on-T phenomenon), which can provoke protracted tachyarrhythmic events, especially in the presence of repolarization abnormalities, such as QT interval prolongation (Fig. 6.5).

Sinus tachycardia is characterized by a heart rate exceeding 100 bpm and P-waves that are normal in both morphology and axis (Fig. 6.6).

This type of tachycardia is characterized by morphologically identical P waves, heart rates ranging from 150 to 250 bpm, and clearly discernible isoelectric lines between the atrial deflections. In most cases, conduction of the atrial impulses to the ventricles is blocked. The AV ratio is usually 2:1 (although 1:1 conduction is by no means rare, which complicates the surface ECG diagnosis), and a Wenckebach pattern is sometimes seen. This arrhythmia is generally the result of increased automaticity, which is manifested by the so-called warm-up phenomenon consisting of progressive rate increases soon after the onset of tachycardia and gradual slowing before it ends (Fig. 6.7). Morphological analysis can often localize the origin of the arrhythmia to the right or left atrium (Figs. 6.8, 6.9, and 6.10).

This supraventricular arrhythmia is characterized by an atrial frequency of >100 bpm and P waves with at least three different configurations (Fig. 6.11). The electrical basis is probably increased automaticity. It is commonly seen in patients with chronic respiratory disease.

Atrial fibrillation (AF) is a very common arrhythmia characterized by chaotic electrical activity in the atria with rates ranging from 350 to 600 bpm. Conduction of the atrial impulses to the ventricles is regulated and slowed by the AV node, which functions as a sort of filter. The ventricular response to the high-rate atrial activity is much lower, generally within the range of 100 to 150 bpm.

ECG diagnosis of AF is usually fairly straightforward. P waves as such are absent: they are replaced by rapid, irregular oscillations of the isoelectric line known as f waves, and the rhythmicity of the ventricular complexes is lost completely (Fig. 6.12). An exception to this rule is AF associated with an atrioventricular block (AVB) (Fig. 6.13): in this case the ventricular complexes occur regularly. As shown in Figs. 6.14 and 6.15, Holter monitoring may reveal phases in which the AVB is even more severe than that seen in Fig. 6.13.

On ECGs recorded during AF (and all other supraventricular arrhythmias as well), there may be morphologically aberrant ventricular complexes, reflecting intermittent or permanent bundle-branch block. When the aberrant complex is isolated and occurs after a short R-R interval preceded by a long R-R interval, it is referred to as an Ashman complex (Fig. 6.16). To understand the Ashman phenomenon, it is important to recall that for myocardial and conduction-system cells, the duration of the refractory periods (i.e., the interval during which the cells have not been repolarized and therefore cannot be re-excited by an external stimulus) generally decreases and increases proportionally with the length of the cardiac cycle. The cells of the AV node are an exception: they behave in the opposite manner and can thus fulfill their role as a filter in the presence of high-frequency atrial activity. The long cycle before an Ashman complex prolongs the refractory period of the bundle-branch cells, and the next complex is widened. The morphology is usually indicative of a block involving the right bundle branch, which normally remains refractory longer than the left bundle branch. When the associated bundle-branch block is permanent, the diagnosis is generally simple (Figs. 6.17, 6.18, and 6.19).

In rare cases, the f waves cannot be clearly visualized on surface tracings: in these cases the differential diagnosis must include atrial standstill, which is characterized by the absence of electrical and mechanical activity in the atria. In some cases, the defect reflects the progression of atrial disease, in others the expression of a genetically determined rhythm disorder (Fig. 6.20).

Three types of AF are usually distinguished:

The association of AF with Wolff-Parkinson-White (WPW) syndrome deserves special mention. In this case, when the electrical impulse is conducted to the ventricles along an accessory pathway, the ventricular complexes are irregular and wide, with varying degrees of aberrancy (see Chap. 7). These features differentiate this form from AF associated with bundle-branch block, which is characterized by constant QRS morphology.

Atrial flutter (AFL) is a type of macro-reentrant atrial tachycardia (Fig. 6.21). Its electrocardiographic features include the absence of P waves and the presence of regular flutter waves (F waves) at rates of 250–350 bpm. As in AF, the AV-node “filter” limits the ventricular response, which rarely exceeds 150–160 bpm. The most common feature of the ECG is a 2:1 block of the impulses arriving from the atria (Figs. 6.22 and 6.23). In this case the nonconducted F wave may be concealed within the QRS complex or occur immediately after it. Poorly visualized F waves can be rendered manifest by interventions that slow atrioventricular conduction (carotid sinus massage, administration of verapamil, digitalis, or adenosine) (Fig. 6.24). There is typically no discernible isoelectric line between the F waves. In general, AFL can be easily diagnosed on a 12-lead surface ECG thanks to the presence of F waves, which are most evident in the inferior leads and in V1.

There are different types of AFL. Data based on intracardiac recordings, particular those obtained during catheter ablation procedures, have increased our understanding of electrophysiological mechanisms. Various AFL classifications have been proposed: one of the most recent is shown in Table 6.2.